This project will study CNS axonal regeneraton in the spinal cord of the postnatal rat and in the visual system of the frog, Rana pipiens, using anatomical methods. These are systems where various factors thought to inhibit CNS regeneration in the mammal are minimized or held constant, while others are varied, and where the success of regeneration differs. 3H-proline and autoradiography and horseradish peroxidase histochemistry (HRP) will be used to anterogradely label developing and regenerating axons. HRP and fluorescent compounds will be used to label the cell bodies of these axons. HRP-filled axons will be studied with the electron microscope. Four different types of experiments will be done. 1) Corticospinal tract (CST) axons of the rat are able to grow around a midthoracic spinal overhemisection made in the newborn and 6 day rat. By comparing the ability of CST axons to grow around this lesion when it is made either at a cervical or a midthoracic level at different ages we will determine if only developing uncut CST axons will grow around this injury or if CST axons will regenerate until the time these axons form synaptic connections. 2) To determine if the immaturity of the CNS during the neonatal period allows axonal regeneration to occur, we will determine the ability of ascending nerve tracts to grow around a midthoracic hemisection made in the newborn rat. We will first determine whether neurons axotomized during the neonatal period survive this injury and study the maturity of the ascending spinal projections at birth. The spinal cord will then be midthoracically hemisected at birth and the ability of ascending nerve tracts to grow around this injury will be analyzed. 3) Optic axons regenerate after middiencephalic hemisection in the frog but tectal efferent axons will not regenerate through this same lesion. We will determine if one factor contributing to this difference is the formation of anomalous synaptic connections near the zone of injury by tectal efferents. 4) Anomalous optic axons regenerate to the opposite retina 4-6 weeks after nerve crush in the frog but later disappear. We will determine if these retino-retinal axons are collaterals of axons which also project to normal contralateral optic targets.